Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/101598
Title: Inhibition of CD200R1 expression by C/EBP beta in reactive microglial cells
Author: Dentesano, Guido
Straccia, Marco
Ejarque Ortiz, Aroa
Tusell Puigbert, José Ma
Serratosa i Serdà, Joan
Saura Martí, Josep
Solà i Subirana, Carme
Keywords: Neurociències
Neurobiologia
Neuròglia
Teixit nerviós
Cultiu de teixits
Neurosciences
Neurobiology
Neuroglia
Nerve tissue
Tissue culture
Issue Date: 2012
Publisher: BioMed Central
Abstract: Background: In physiological conditions, it is postulated that neurons control microglial reactivity through a series of inhibitory mechanisms, involving either cell contact-dependent, soluble-factor-dependent or neurotransmitter-associated pathways. In the current study, we focus on CD200R1, a microglial receptor involved in one of these cell contact-dependent mechanisms. CD200R1 activation by its ligand, CD200 (mainly expressed by neurons in the central nervous system),is postulated to inhibit the pro-inflammatory phenotype of microglial cells, while alterations in CD200-CD200R1 signalling potentiate this phenotype. Little is known about the regulation of CD200R1 expression in microglia or possible alterations in the presence of pro-inflammatory stimuli. Methods: Murine primary microglial cultures, mixed glial cultures from wild-type and CCAAT/enhancer binding protein β (C/EBPβ)-deficient mice, and the BV2 murine cell line overexpressing C/EBPβ were used to study the involvement of C/EBPβ transcription factor in the regulation of CD200R1 expression in response to a proinflammatory stimulus (lipopolysaccharide (LPS)). Binding of C/EBPβ to the CD200R1 promoter was determined by quantitative chromatin immunoprecipitation (qChIP). The involvement of histone deacetylase 1 in the control of CD200R1 expression by C/EBPβ was also determined by co-immunoprecipitation and qChIP. Results: LPS treatment induced a decrease in CD200R1 mRNA and protein expression in microglial cells, an effect that was not observed in the absence of C/EBPβ. C/EBPβ overexpression in BV2 cells resulted in a decrease in basal CD200R1 mRNA and protein expression. In addition, C/EBPβ binding to the CD200R1 promoter was observed in LPS-treated but not in control glial cells, and also in control BV2 cells overexpressing C/EBPβ. Finally, we observed that histone deacetylase 1 co-immunoprecipitated with C/EBPβ and showed binding to a C/EBPβ consensus sequence of the CD200R1 promoter in LPS-treated glial cells. Moreover, histone deacetylase 1 inhibitors reversed the decrease in CD200R1 expression induced by LPS treatment. Conclusions: CD200R1 expression decreases in microglial cells in the presence of a pro-inflammatory stimulus, an effect that is regulated, at least in part, by C/EBPβ. Histone deacetylase 1 may mediate C/EBPβ inhibition of CD200R1 expression, through a direct effect on C/EBPβ transcriptional activity and/or on chromatin structure.
Note: Reproducció del document publicat a: http://dx.doi.org/10.1186/1742-2094-9-165
It is part of: Journal of Neuroinflammation, 2012, vol. 9, num. 165
Related resource: http://dx.doi.org/10.1186/1742-2094-9-165
URI: http://hdl.handle.net/2445/101598
ISSN: 1742-2094
Appears in Collections:Articles publicats en revistes (Biomedicina)

Files in This Item:
File Description SizeFormat 
617319.pdf808.97 kBAdobe PDFView/Open


This item is licensed under a Creative Commons License Creative Commons